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AJP - Heart and Circulatory Physiology, Vol 266, Issue 6 2462-H2467, Copyright © 1994 by American Physiological Society
ARTICLES |
A. P. Williamson, E. Seifen, J. P. Lindemann and R. H. Kennedy
Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock 72205.
This study was designed to determine the role of the alpha 1-adrenergic receptor (AR) subtypes in the positive inotropic action of alpha 1-adrenergic agonists in rat myocardium. Isolated left atrial and papillary muscle were suspended in oxygenated Krebs-Henseleit buffer (37 degrees C) containing 3 microM nadolol and paced at 3.3 Hz. Isometric tension was continuously monitored. Cumulative concentration-response curves for phenylephrine (3 x 10(-7) to 3 x 10(-4) M) were obtained in the presence and absence of WB4101 (4 and 10 nM) and with and without treatment with chloroethylclonidine (CEC; 10, 100, and 300 microM). WB4101 antagonized the effect of phenylephrine in both tissues, increasing half-maximal effective concentration (EC50) values in a concentration-dependent manner. CEC pretreatment also increased EC50 values in both tissues, and 300 microM CEC reduced the maximal positive inotropic effect of phenylephrine by approximately 48 and 38% in left atrial and papillary muscle, respectively. CEC alone elicited significant increases in contractile force that were not readily reversible. These data suggest that the positive inotropic effect of alpha 1-adrenergic agonists in rat atrial and ventricular myocardium results from stimulation of both WB4101- and CEC-sensitive alpha 1-ARs.
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S. J. Liu and R. H. Kennedy alpha 1-Adrenergic activation of L-type Ca current in rat ventricular myocytes: perforated patch-clamp recordings Am J Physiol Heart Circ Physiol, June 1, 1998; 274(6): H2203 - H2207. [Abstract] [Full Text] [PDF] |
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